Chlo pathologies. Specific inflammatory diseases of the maxillofacial area. When should you contact an oral and maxillofacial surgeon?

Every day, dentists or maxillofacial surgeons are faced with the issues of making a diagnosis based on a clinical examination, determining the location of the source of the disease and diagnostics that establish the differences between the existing disease and others. Specialists must quickly assess the degree of damage, the patient’s physical well-being and psycho-emotional state. The doctor must anticipate the possible course of advanced inflammatory processes.

Dentists of the new generation with a high degree of clinical education, well-read, and good thinking abilities successfully solve the problems of complex patients. This became especially noticeable in circumstances where anti-inflammatory drugs and sulfonamides, having played the leading role, did not justify the trust of doctors. While exhibiting a therapeutic effect, these drugs destroy the body's defenses.

Causes of inflammation of the maxillofacial area

Currently, there is a rise in odontogenic inflammatory diseases. In children, the disease occurs more often than in older people, this is explained by the immunobiological characteristics of the body. Inflammatory diseases of odontogenic etiology take a long time and are difficult to treat.

This process is a consequence of carious diseases of the oral cavity and the result of complicated forms of the disease. The specific microflora of the carious process contributes to the severity of the odontogenic inflammatory disease. The inflammatory process can be nonspecific and specific. Nonspecific inflammation is caused by anaerobic microflora. According to the method of progression, acute and chronic processes and subacute forms are distinguished. The most common is the subacute form, which is more common in children. Pathologies arise in the absence of timely and high-quality treatment, injuries, hematogenous and odontogenic infections.

There are three views on the classification of inflammatory diseases in the maxillofacial area. Studying various manifestations of acute odontogenic inflammatory diseases, the famous scientist G. A. Vasiliev established some of their features. He managed to divide the processes into periodontitis, periostitis, osteomyelitis, abscesses and phlegmon.

Diseases with predominant damage to the bone structures of the jaw

Inflammation of the bone structures of the jaws occurs due to bone damage from external influences, the presence of inflammation, cystic changes or tumor growth. Inflammation affects bones, periosteum and even bone marrow. The causes of the pathology are an acute inflammatory process at the apex of the root of the causative tooth, an exacerbation of sluggish periodontitis or periodontal disease.

Tumors are classified as odontogenic and non-odontogenic. They are benign and malignant. The jaw bones can be affected by cancer metastases.

Acute or chronic periodontitis in the acute stage

Acute periodontal inflammation is expressed by severe spontaneous pain, which intensifies when pressing or tapping on the tooth. Swelling, infiltration along the transitional fold and painful staticity appear. At the same time, the general condition of the body suffers: a slight increase in body temperature over a long period and an increase in regional lymph nodes. The clinic of a sluggish process does not have clear symptoms. The main inconvenience is caused by eating and halitosis. Along the transitional fold, a pathological channel may appear for the outflow of secretions from the source of inflammation, which begins in the carious cavity of a destroyed tooth or in a restored tooth. The following classification is used:

• periodontitis of the root apex (apical);
• marginal (marginal) periodontitis.

Marginal periodontitis is considered a disease of the tissues surrounding the tooth root. Therapy of aggravated sluggish processes and acute suppurations follows one method. First aid is to create a free outflow of purulent discharge from the canals of the affected tooth.

Apical periodontitis leads to a defect in the ligamentous apparatus of the tooth and bone destruction. In some cases, jaw fracture may develop.

After the inflammatory processes have been eliminated, endodontic and antimicrobial-instrumental treatment is carried out. The same principle is used to treat chronic forms of periodontitis. Impregnation and physical methods can also be used.

Acute odontogenic osteomyelitis

Damage to the bone marrow of the upper and lower jaw is commonly called osteomyelitis in dentistry. The development of the disease depends on the method of introduction of pathological microflora into the bones and the course of the inflammatory process.

Inflammation of the bone marrow of the jaw bones has its own classification:

• acute infection (odontogenic) - 80% of all diseases;
• penetration of infection from the bloodstream (hematogenous) - 9% of cases;
• penetration of infection from the traumatic focus - 11%.

Classification according to the clinical course of osteomyelitis and the results of x-ray examination is as follows:

• destroying bone structure (destructive form);
• destroying the bone structure with its subsequent restoration;
• a productive type of osteomyelitis, which forms new layers after the inflammatory process.

The acute course of osteomyelitis begins with the penetration of pathogenic microflora into the site of bone inflammation, damage to its entire structure and purulent melting. Bone nutrition is disrupted, followed by necrosis. The clinical picture of the acute osteomyelitic process is accompanied by an increase in the patient’s body temperature, the appearance of chills and general pain.

In the first days of the disease, no changes are noted in the photographs of the jaws. After seven or more days, a focus of bone loss appears, which is the result of purulent melting of the bone. Its transparency is due to the disappearance of the lamellar pattern, thinning and rupture of the cortical plate. Osteomyelitis of the upper jaw of odontogenic etiology is rarely indolent. The acute development of the disease is due to the anatomical and physiological structure of the upper jaw, the rapid opening of the abscess and the abrupt end of the process.

Diseases with predominant damage to the perimaxillary soft tissues

Diseases of the maxillofacial area caused by pathogenic microflora of decayed teeth are called odontogenic diseases. They affect not only the bones, but also the regional lymphatic system. The manifestations of symptoms depend on the general condition of the patient, the degree of pathogenicity of the microflora at the site of inflammation, the location of the causative tooth and the prevalence of the inflammatory process.

Odontogenic periostitis

The inflammatory process of the periosteum is called periostitis. Its cause is diseased teeth or their poor treatment, inflammation of the pulp (acute or chronic), purulent processes in perihilar cysts, pericoronaritis of permanent and primary occlusion, external mechanical influence.

There are acute serous and acute purulent periostitis. The chronic process can be simple and occur with bone compaction.

Acute serous periostitis is manifested by swelling of the vestibular fold with painful palpation. There is pronounced redness of the mucous membrane above the site of swelling. The process is concentrated in the area of ​​the affected tooth and adjacent teeth, with the predominant localization of inflammatory exudate along the transitional fold.

Acute purulent periostitis is characterized by increased swelling of the vestibular surface and the development of an organized inflammatory process in the subperiosteal space. With a violation of the integrity of the periosteum and the leakage of purulent exudate. Over the accumulation of fluid in the resulting cavity, oscillations, redness of the mucous membrane in the mouth and the skin on the outside, and local compaction are detected.

Chronic periostitis is manifested by bone growth due to increased proliferative process in the periosteum of varying degrees of ossification (we recommend reading: linear periostitis: symptoms and treatment methods). In childhood, bones are in constant physiological irritation due to teething and jaw growth.

Pericoronitis

Inflammation of the gums is called pericoronitis. The process occurs with severe pain in the area of ​​the erupting tooth, jaw lockjaw of varying degrees, pain when swallowing, and halitosis. The patient's general condition suffers. Inflammation of the mucous hood during teething occurs due to the concentration of soft plaque in the resulting gum defect. Wisdom tooth dystopia leads to the formation of pathological processes in the dental arch: destruction of a nearby tooth, development of traumatic stomatitis, inflammation of the bone in the growth area of ​​the “eight”.

Odontogenic abscess

An abscess is a local purulent inflammation limited to the capsule that occurs during acute or chronic focal infection. It begins with inflammation of the facial skin, with stomatitis of various etiologies, cheilitis, rhinitis, conjunctivitis and traumatic interventions.

Abscesses of the maxillo-oral cavity are the most common. They begin with inflammatory processes in the causative tooth. In the problem area, the skin is thinned, the patient experiences pain during palpation and feels the fluid swaying under the skin. The general condition has not changed.

Phlegmon

Cellulitis is a local inflammation accompanied by redness, painful swelling and enlargement of local lymph nodes. Treatment begins with surgical intervention, then drainage is performed, and the inflammation site is washed with antiseptic solutions. If necessary, complex therapy is prescribed. The rapid development of the process in pediatric practice is due to poorly developed subcutaneous connective tissue and poor connection with the subcutaneous fat and capillary layer. This is the etiology of the rapid development of the process, complicated by poorly developed defenses of the body.

Odontogenic inflammatory infiltrate

Local compaction of soft tissues, an increase in their volume due to the accumulation of blood cells, lymph and other elements in the inflamed area - these are all manifestations of odontogenic inflammatory infiltrate. Some experts call the infiltration process “incipient phlegmon.” Odontogenic infected inflammation of the serous type is completely eliminated with the help of complex therapy. Infiltrative processes are considered as a local reaction. When making a diagnosis, it is important to distinguish serous inflammation from purulent inflammation and carry out high-quality therapy.

Diseases with predominant damage to the regional lymphatic system

Most often, with odontogenic inflammatory diseases, the submandibular lymph nodes are affected. Studies have shown that in most patients (more than 60%) the submandibular lymph nodes were affected. The chin is affected less frequently (about 9%). The disease can also affect the buccal, parotid and cervical lymph nodes. The most common is lymphadenitis, less often - adenophlegmon. There is a separate group of inflammatory diseases of the maxillofacial area. This includes a disease such as actinomycosis. Specific diseases affect the lymph nodes and can occur against the background of odontogenic inflammatory diseases.

Odontogenic lymphadenitis (serous, purulent)

Lymphadenitis often occurs against the background of other diseases (for more details, see the article: submandibular lymphadenitis in children and adults). Any infections, acute respiratory infections or acute respiratory viral infections, as well as diseases of the ENT organs can provoke lymphadenitis at any time. Often doctors attribute it to one of the symptoms. There are often cases when inflammation is caused by hypothermia, trauma, or occurs after vaccination. Depending on the clinical course, lymphadenitis is divided into: serous, purulent or chronic.

A rapid course of the disease with the manifestation of local symptoms and a pronounced reaction of the body is noted in acute serous lymphadenitis. A patient with a high temperature begins to show signs of intoxication. At the initial stage, there is a slight increase in lymph nodes, which upon palpation cause pain to the patient. Lymph nodes can be mobile, but dense; the skin at the site of inflammation does not change color. If appropriate measures are not taken at this stage, lymphadenitis enters the next stage with damage to the soft tissue surrounding the lymph nodes (periadenitis). When palpating a lymph node, a person experiences sharp pain, and an infiltrate is felt at the site of inflammation. Subsequently, acute purulent lymphadenitis occurs with the release of purulent exudate.

In the chronic course of the disease, the lymph node is palpated as mobile, dense, painless, but in some cases the patient may experience discomfort. With chronic abscessive lymphadenitis, a fistula may form with the release of purulent contents.

Adenophlegmon

Children are more often susceptible to adenophlegmon, but it can occur as a result of lymphadenitis in patients of all ages. Even young children, starting from two months, can experience unpleasant symptoms of the disease. Most often, adenophlegmon affects the buccal and submandibular lymph nodes. Less commonly localized in the chin and parotid region.

The most common sources of the development of the disease are: untreated teeth, inflammation of the ENT organs, and trauma. Adenophlegmon has severe symptoms, and the patient experiences increasing intoxication. By palpation, the focus of inflammation is determined as an infiltrate. The skin in the affected area becomes dense, tense, and hyperemic.

Complications of odontogenic inflammatory diseases

Sometimes inflammation in the maxillofacial area leads to serious life-threatening complications. They often manifest themselves in the form of mediastinitis, thrombophlebitis of the facial veins, thrombosis and intracranial processes. Such complications in the maxillofacial area are associated with the spread of infection to vital organs: the mediastinal area, the brain. Intracranial complications require immediate treatment, as there is mortality associated with severe disease. According to statistics, 20%-60% of people die.

Mediastinitis

Mediastinitis develops in patients against the background of the development of phlegmon. Odontogenic infection can quickly spread from the maxillofacial region to the mediastinum from the periglottic space and the root of the tongue to the retroglottic, and then to the pharynx and esophagus. The infection first affects the posterior mediastinum, and then moves to the anterior.

Mediastinitis in the presence of phlegmon can be detected by the following signs:

• the inflammatory process is localized in the cervical region;
• drainage of purulent foci does not bring the desired result, the patient has a high temperature and tachycardia.

The main symptoms of mediastinitis:

1. In a patient, upon palpation, inflammatory infiltrates are determined in the places where the neurovascular bundle passes.
2. The patient is always in a sitting position with his head bowed or lying down with his knees drawn up.
3. At rest, the patient experiences shortness of breath.
4. The Ravich-Scherbo symptom appears.
5. The patient coughs, sighs and throws his head back, experiencing pain. Gradually they intensify.
6. Due to hypersecretion of mucus, the patient begins to cough, accompanied by pain.
7. When the doctor taps certain areas, in particular the sternum and heels, the patient experiences pain.
8. On x-rays, the shadow of the mediastinum increases in size, and with a purulent infection, the presence of gas in the retrosternal space is revealed.

Thrombophlebitis of facial veins, dural sinuses

The main manifestation of thrombophlebitis is the formation of infiltrates, changes in skin color, and the appearance of edema that spreads beyond the infiltrates along the angular or facial vein. The body temperature rises, a blood test indicates an inflammatory process in the body.

One of the complications of thrombophlebitis is thrombosis of the cavernous sinus. This inflammation occurs inside the skull. The patient complains of severe headaches, body temperature can reach 38-40 degrees. ESR increased to 40-60 mmh. The disease is accompanied by swelling and hyperemia in the eyelids, forehead, and fundus. The pupils are dilated. In some patients, the neck muscles become stiff.

In children, this disease can occur due to dehydration and fever. There are also frequent cases of sinus thrombosis due to complications caused by sickle cell anemia, severe cachexia, erythrocytosis and leukemia. Sometimes the disease occurs in women in the postpartum period and is associated with oral contraceptives.

Meningitis, meningoencephalitis, brain abscess

In cases of melting of the walls of the cavernous sinus caused by thrombosis, the patient experiences another type of complication - purulent meningitis. This complication is accompanied by a rapid rise in body temperature, headaches, nausea, and vomiting. The person is in a depressed state, his neck muscles become rigid, and changes in the cerebrospinal fluid are noted.

Meningoencephalitis in its clinical picture is similar to meningitis; its distinctive feature is the addition of focal symptoms. The person may lose consciousness. This complication is accompanied by tachycardia, arrhythmia, and low blood pressure.

What is the competence of a maxillofacial surgeon?

What diseases does the Maxillofacial Surgeon deal with?

1) Inflammatory diseases of the teeth, jaws, tissues of the face and neck, oral organs (periodontitis, periostitis, osteomyelitis of the jaw, abscesses, phlegmon, lymphadenitis, difficult teething, odontogenic inflammation of the maxillary sinus, inflammatory diseases of the salivary glands, temporomandibular joint ).

2) Injuries to the soft tissues of the face and neck, bones of the facial skeleton.

3) Tumors and tumor-like formations of the face, jaws, and oral cavity organs.

4) Congenital and acquired defects and deformations of the face, jaws and plastic surgeries of the maxillofacial area (blepharoplasty, otoplasty, rhinoplasty, circular facelift, contour plastic surgery).

What organs does the maxillofacial surgeon deal with?

When should you contact an Oral and Maxillofacial Surgeon?

The affected tooth is discolored and mobile. It may have a carious cavity, or it may be intact.

Probing is painless, but the reaction to percussion is sharply painful. The mucous membrane in the area of ​​the transitional fold is swollen, hyperemic, and painful on palpation.

As the process progresses, swelling of the soft tissues may occur, leading to facial asymmetry, and the general condition is disturbed (headache, weakness, malaise, body temperature rises to 38 - 39 ° C). There is an increase and swelling of the regional lymph nodes.

The symptoms of periostitis - inflammation of the periosteum of the jaw - are well known to many children and adults: a sharply painful hard compaction appears on the gum near a tooth with dead pulp or the remaining root, rapidly increasing.

The swelling, becoming more pronounced, spreads to the soft tissues of the face. Depending on the location of the diseased tooth, the lip and wing of the nose, cheek and lower eyelid swell, the temperature rises, and the person feels unwell. This disease is popularly known as flux.

Symptoms of osteomyelitis of the jaws

spontaneous throbbing pain in the jaw, headache, chills, temperature up to 40 "C. An affected tooth with a necrotic pulp (possibly with a filling) is found; it and the adjacent teeth are sharply painful and mobile. A swollen asymmetrical face. The transitional fold is hyperemic and smoothed. Lymph nodes are enlarged and painful.

Osteomyelitis is often complicated by an abscess and phlegmon. In the blood there is neutrophic leukocytosis; ESR is increased. General condition of varying severity.

An abscess is a limited accumulation of pus in various tissues and organs. An abscess should be distinguished from phlegmon (spread purulent inflammation of tissues) and empyema (accumulation of pus in body cavities and hollow organs).

General clinical manifestations of abscesses are typical for purulent-inflammatory processes of any localization: increased body temperature from subfebrile to 41° (in severe cases), general malaise, weakness, loss of appetite, headache.

Leukocytosis with neutrophilia and a shift of the leukocyte formula to the left is noted in the blood. The extent of these changes depends on the severity of the pathological process.

In the clinical picture of abscesses of various organs there are specific signs determined by the localization of the process. The outcome of an abscess can be a spontaneous opening with a breakthrough to the outside (subcutaneous tissue abscess, mastitis, paraproctitis, etc.); breakthrough and emptying into closed cavities (abdominal, pleural, joint cavity, etc.); breakthrough into the lumen of organs communicating with the external environment (intestines, stomach, bladder, bronchi, etc.). Under favorable conditions, the emptied abscess cavity decreases in size and undergoes scarring.

If the abscess cavity is not completely emptied and its drainage is poor, the process can become chronic with the formation of a fistula. The breakthrough of pus into closed cavities leads to the development of purulent processes in them (peritonitis, pleurisy, pericarditis, meningitis, arthritis, etc.).

Lymphadenitis is inflammation of the lymph nodes.

Acute lymphadenitis almost always occurs as a complication of a local source of infection - a boil, an infected wound or abrasion, etc. Infectious agents (usually staphylococci) penetrate the lymph nodes with the flow of lymph through the lymphatic vessels, often without inflammation of the latter, i.e. without lymphagiitis.

Purulent foci on the lower extremity are complicated by damage to the inguinal, less often popliteal lymph nodes; on the upper limb - axillary, less often elbow, on the head, in the oral cavity and pharynx - cervical.

When and what tests should be done

What are the main types of diagnostics usually performed by a Maxillofacial Surgeon?

When implanting teeth, special implants are used that are installed in the area of ​​missing teeth.

A titanium “screw” is screwed into the bone, onto which the crown is fixed. The materials for implants are titanium and its alloys, tantalum, various types of ceramics, leucosapphire, zirconium and other substances. All these materials are highly bioinert, that is, they do not cause irritation to surrounding tissues.

Benefits of implantation

Neighboring teeth are not ground down;
- a defect of any length can be restored;
- strength and reliability (the service life of implants is longer than with other types of prosthetics, since the very first implants installed more than 40 years ago continue to serve their owners);
- high aesthetics (the implant is practically indistinguishable from a healthy natural tooth).

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Purulent-inflammatory diseases of the maxillofacial area, despite the successes achieved in the diagnosis and treatment of this pathology in recent years, have not lost their scientific and practical significance and remain one of the leading problems of maxillofacial surgery. This is due to the increasing number of patients with odontogenic purulent diseases maxillofacial region (MGZ MFA), the number of which in maxillofacial hospitals reaches more than 50%, changes in the clinical course of the pathological process and an increase in severe forms and spread to adjacent cellular spaces, as well as life-threatening complications: contact mediastinitis, sepsis, cavernous thrombosis sinus, brain abscess, etc., damage to the organs of the ear, nose and throat (ENT organs), orbit, leading in severe cases to loss of vision and even death. In this regard, the diagnosis of purulent-inflammatory diseases of the maxillofacial area (PVD of the maxillofacial area) goes beyond the competence of the maxillofacial surgeon and becomes important for general and thoracic surgeons, ophthalmologists, otorhinolaryngologists and neurosurgeons.

The increase in the number of cases of acute respiratory infections is due to a significant decrease in the quality of life of the population, material and living conditions, deterioration of nutrition, lack of planned sanitation, decrease in the level and quality of personal hygiene, which contribute to a decrease in general resistance and nonspecific immunity and an increase in the level of dental morbidity and cases of chronic odontogenic infection.

Classification. The most widespread, taking into account clinical manifestations and topographic anatomy, is the classification of phlegmon by A. I. Evdokimov (1964), according to which there are phlegmon of the face, perimandibular phlegmon, phlegmon of the floor of the mouth, tongue and neck. GVZ of the maxillofacial area were systematized in the works of V. F. Voino-Yasenetsky (1956), V. S. Dmitrieva (1969), V. I. Lukyanenko, V. A. Kozlov (1988), M. M. Solovyov and O. P Bolshakova (1997).

In a generalized form, the classification of intravenous lesions of the maxillofacial area can be presented as follows:

By etiology:

• nonspecific;
• anaerobic;
• anaerobic-aerobic;
• aerobic;
• specific: actinomycosis, syphilis.

• odontogenic;
• non-odontogenic: traumatic, hematogenous, lymphogenic, iatrogenic.

• bone tissue: periodontitis, periostitis, pericoronitis, periodontitis, osteitis, osteomyelitis;
• soft tissues: abscess, phlegmon, adenophlegmon, odontogenic subcutaneous granuloma.

• cellulite;
• fasciitis;
• myositis (myonecrosis).

• limited;
• spilled (polyphlegmon).

• superficial;
• deep.

• upper face area;
• middle zone of the face;
• lower face area;
• lateral areas of the face;
• organs and tissues of the oral cavity;

In various inflammatory diseases of the maxillofacial region, obligate anaerobes are found in 90% of cases, with associations of obligate anaerobes in 25-30% of cases, associations of anaerobes and aerobes in 60-65% of cases, and aerobes in 10% of cases.

In the 1960-1970s. The main attention as the causative agents of gastrointestinal tract infection was given to epidermal and Staphylococcus aureus and hemolytic streptococci. In the 1980s the use of strict anaerobic technology made it possible to identify representatives of obligate non-spore-forming anaerobes: bacteroides, fusobacteria, peptococci, peptostreptococci, anaerobic streptococci, veillonella, volinella, involved in the development of purulent-necrotic lesions of the maxillofacial area.

In the pathogenesis of various inflammatory diseases of the maxillofacial region, there are different ways of penetration of microflora into the site of inflammation. Thus, with odontogenic osteomyelitis and phlegmon, the entrance gates of infection are teeth, with traumatic osteomyelitis - ruptures of the mucous membrane due to fractures of the jaw bones, and with adenophlegmon - the lymphatic route. Obligate anaerobes in the process of life produce toxins and “aggressive” enzymes that promote the creeping infiltrating spread of infection from the primary focus to adjacent areas where aerobes colonize already necrotic tissues. Purulent-necrotic tissue lesions in 66.7% of cases occur as cellulite, in 12.5% ​​as fasciitis, and in 20.8% as myonecrosis.

Consequently, the penetration of anaerobes into the tissues of the maxillofacial area is facilitated by teeth affected by complicated caries, injuries, as well as instrumental manipulations, surgical interventions, and local tissue changes.

There are a number of theories about the pathogenesis of purulent-inflammatory diseases of the maxillofacial area: the embolic theory of A. A. Bobrov (1889) and Lexer (1894), which explains the spread of infection in emboli and thrombosis of capillaries; allergic theory of S. M. Derizhanov (1940), Ya. M. Snezhko (1951), which determines the leading role of sensitization of the body based on the Arthus-Sakharov phenomenon; reflex theory of G.I. Semenchenko (1958), emphasizing the importance of the nervous system in the development of neurotrophic disorders leading to the development of the inflammatory process.

In recent years, significant additions have been made to the development of the pathogenesis of maxillofacial lesions. A number of authors have identified significant changes in the hemostasis system, leading to an increase in the hypercoagulability syndrome, qualitative changes in fibrinogen, its loss in the form of fibrin, which contributes to intravascular coagulation and disruption of microcirculation with subsequent tissue necrosis and purulent melting (Gruzdev N. A., 1978; Balin V.N., 1987, etc.). In recent decades, significant importance in the development of GVD of the maxillofacial area has been given to the reduction of general and local resistance of the human body and the development of secondary immunodeficiency (Soloviev M. M., 1971; Robustova T. G., 1990; Shargorodsky A. G., 2004). A decrease in the body’s nonspecific defense mechanisms is associated with hypothermia, overwork, stressful situations, viral and other infections, concomitant and background diseases: diabetes, blood diseases, liver, kidneys, rheumatism, cancer, etc.; chemotherapy. In recent years, great importance has been attached to the state of the body's antioxidant system (AOS) in the development of intravenous diseases of the maxillofacial area, disruption of the links of which leads to changes in the most important physiological functions of the body.

"Diseases, injuries and tumors of the maxillofacial region"
edited by A.K. Iordanishvili

Inflammatory diseases of the maxillofacial region, and in particular, severe forms of odontogenic inflammatory processes are periodontitis, periostitis, osteomyelitis of the jaws and phlegmon of the surrounding soft tissues. For questions of their etiology and pathogenesis, see the textbook: Therapeutic Dentistry. Ed. E.V. Borovsky. – M.: Medicine, 1989 and Surgical dentistry. Ed. T.G.Robustova. – M.: Medicine, 1990.

Features of the occurrence and course of inflammatory reactions in the tissues of the oral cavity:

Inflammatory processes in the maxillofacial region are characterized by granulomatous inflammation, which is characterized by a limited focus of productive, productive-exudative inflammation, and the formation of limited infiltrates. This inflammation is based on primary growths of granulation tissue infiltrated with polynuclear cells, lymphocytes, and plasma cells in various proportions. An example of such inflammation is dental granuloma - a tumor-like formation near the apex of the tooth made of granulation tissue, surrounded by a fibrous capsule, resulting from chronic inflammation during infection of the periodontium from the tooth canal. In cases of development of inflammatory processes in the maxillofacial area, it is necessary to remember the characteristics of the venous system. The absence of a valve system in the veins of the face makes it possible for a thrombus to rapidly migrate in an ascending direction and cause thrombosis of the peritoneal sinus with an extremely life-threatening prognosis for patients.

Features of changes in the white blood system and hemostasis disorders during inflammatory processes in the tissues of the oral cavity.

Comparative studies of capillary blood of the gums and fingers in people suffering from inflammatory processes in the maxillofacial area (gingivitis, periodontal disease, etc.) revealed statistically significant changes in the composition of leukocytes. These changes concern the absolute number of eosinophils, neutrophils, lymphocytes and monocytes, as well as the total number of leukocytes. In the capillary blood of the gums, the number of phagocytes (eosinophils, neutrophils and monocytes) is significantly lower and the number of immunocompetent cells (lymphocytes) increases. A decrease in the phagocytic activity of neutrophils was revealed (especially in periodontal disease). Since phagocytes are one of the main factors of nonspecific immunity, a decrease in their total number in the gums during inflammatory processes of the oral cavity suggests that these processes develop against the background of a decrease in the body’s nonspecific immune response.

Features of hemostasis in pathology of the oral cavity are determined by the presence in the saliva of the oral fluid of plasma components of the coagulation, fibrinolytic and kallikrein-kinin systems, their various quantitative and qualitative disorders, and changes in their combination.

In chronic inflammatory processes of the oral cavity, with periodontal disease, the content of proteinase inhibitors in the oral fluid decreases, the activity of the proteolytic enzyme system increases, which leads to an increase in the activity of plasmin, thrombin, kallikrein, blood coagulation factors and is manifested by activation of the coagulation, fibrinolytic and kallikreinin systems. Such hemostasis disorders serve as the basis for pathological processes that clinically manifest themselves in the form of blood vessel thrombosis. The absence of a valve system in the veins of the face makes it possible for a blood clot to migrate rapidly in an upward direction. The intimate connection of the venous formations of the maxillofacial region with the pterygoid plexus, and the latter through the middle veins of the dura mater with the cavernous sinus of the dura mater, with the development of thrombosis, can cause a severe complication in the form of thrombosis of the cavernous sinus with an extremely life-threatening prognosis. Therefore, these features of hemostasis in oral pathology must be taken into account when analyzing the patient’s condition and developing doctor’s tactics in cases of the development of inflammatory and other processes in the maxillofacial area.

The role of local hypoxia in the pathogenesis of inflammatory and dystrophic lesions of tissues of the maxillofacial region.

In the development of inflammatory and dystrophic lesions of the tissues of the maxillofacial area (gingivitis, inflammatory-dystrophic form of periodontal disease, etc.), the most pronounced changes occur in the capillary, precapillary and arterial parts of the microvasculature, which leads to hypoxia, metabolic disorders and dystrophic changes in the pulp and periodontium. Against the background of dystrophic tissue damage (periodontal tissue) during chronic hypoxia, regenerative processes sharply decrease. Inhibition of proliferative processes is caused by insufficient energy supply to tissues and is associated with excessive formation of glucocorticoids, which suppress proliferation processes and lengthen all phases of the cell cycle.

In clinical and, in particular, dental practice, for diseases of the oral mucosa and periodontal disease, treatment with oxygen under high pressure - 3 atm is recommended. (hyperbaric oxygen therapy). The therapeutic effect of hyperbaric oxygenation is based on an increase in the partial pressure of oxygen in body fluids (plasma, lymph, interstitial fluid). This leads to a corresponding increase in their oxygen capacity (by 6.5%) and is accompanied by an increase in the diffusion of oxygen in the hypoxic area of ​​​​tissues, which helps to normalize the arteriovenous difference in oxygen, i.e. oxygen consumption by the body at rest.

In the maxillofacial region, a special group consists of inflammatory diseases caused by specific pathogens: radiant fungus, Treponema pallidum, Mycobacterium tuberculosis. Diseases caused by these pathogens (actinomycosis, syphilis, tuberculosis) are usually classified into the group of specific inflammatory processes.

ACTINOMYCOSIS

Actinomycosis, or radiant fungal disease, is an infectious disease that occurs as a result of the introduction of actinomycetes (radiant fungi) into the body. The disease can affect all organs and tissues, but more often (80-85% of cases) the maxillofacial area.

Etiology. The causative agents of actinomycosis are radiant fungi (bacteria). The culture of actinomycetes can be aerobic or anaerobic. In actinomycosis in humans, in 90% of cases, the anaerobic form of radiant fungi (proactinomycetes) is isolated, less often - certain types of aerobic actinomycetes (thermophiles) and micromonospores. In the development of actinomycosis, a significant role is played by a mixed infection - streptococci, staphylococci, diplococci and other cocci, as well as anaerobic microbes - bacteroides, anaerobic streptococci, staphylococci, etc. Anaerobic infection helps the penetration of actinomycetes into the tissues of the maxillofacial area and their further spread throughout the cellular spaces .

Pathogenesis. Actinomycosis occurs as a result of autoinfection, when radiant fungi penetrate the tissues of the maxillofacial region, and a specific actinomycosis granuloma or several granulomas are formed. In the oral cavity, actinomycetes are found in dental plaque, carious dental cavities, pathological periodontal pockets, and on the tonsils; actinomycetes constitute the main stroma of dental calculus.

The development of the actinomycosis process reflects complex changes in the immuno-biological reactivity of the body, nonspecific defense factors in response to the introduction of an infectious agent - radiant fungi. Normally, the constant presence of actinomycetes in the oral cavity does not cause an infectious process, since there is a natural balance between the immunological mechanisms of the body and the antigens of radiant fungi.

The leading mechanism for the development of actinomycosis is a disorder of the immune system. For the development of actinomycosis in the human body, special conditions are required: a decrease or disruption of the body’s immunobiological reactivity, a nonspecific defense factor in response to the introduction of an infectious agent - radiant fungi. Among the common factors that impair immunity are primary or secondary immunodeficiency diseases and conditions. Local pathogenetic causes are of great importance - odontogenic or stomatogenic, less often - tonsillogenic and rhinogenic inflammatory diseases, as well as tissue damage that disrupts the normal symbiosis of actinomycetes and other microflora. With actinomycosis, specific immunity disorders and immunopathology phenomena develop, of which the leading one is allergy.

The entrance gates for the introduction of actinomycosis infection when tissues and organs of the maxillofacial area are damaged can be carious teeth, pathological periodontal pockets, damaged and inflamed mucous membrane of the oral cavity, pharynx, nose, ducts of the salivary glands, etc.

Actinomycetes spread from the site of introduction by contact, lymphogenous and hematogenous routes. Typically, a specific focus develops in well-vascularized tissues: loose tissue, connective tissue layers of muscles and bone organs, where actinomycetes form colonies - drusen.

The incubation period ranges from several days to 2-3 weeks, but can be longer - up to several months.

Pathological anatomy. In response to the penetration of radiant fungi into tissue, a specific granuloma is formed. Directly around the colonies of the radiant fungus – drusen of actinomycetes, polynuclear cells and lymphocytes accumulate. Along the periphery of this zone, granulation tissue rich in thin-walled small-caliber vessels is formed, consisting of round, plasma, epitheloid cells and fibroblasts. Giant multinucleated cells are also occasionally found here. The presence of xanthoma cells is characteristic. Subsequently, in the central parts of the actinomycosis granuloma, necrobiosis of cells and their disintegration occurs. In this case, macrophages rush to the colonies of drusen of the radiant fungus, capture pieces of mycelium and migrate with them to the tissues adjacent to the specific granuloma. A secondary granuloma forms there. Further, similar changes are observed in the secondary granuloma, a tertiary granuloma is formed, etc. Daughter granulomas give rise to diffuse and focal chronic infiltrates. Along the periphery of a specific granuloma, granulation tissue matures and turns into fibrous tissue. At the same time, the number of vessels and cellular elements decreases, fibrous structures appear, and dense scar connective tissue is formed.

Morphological changes in actinomycosis are directly dependent on the reactivity of the body - factors of specific and nonspecific protection. This determines the nature of the tissue reaction - the predominance and combination of exudative and proliferative changes. The addition of a secondary pyogenic infection is of no small importance. Intensification of necrotic processes and local spread of the process are often associated with the addition of purulent microflora.

Clinical picture The disease depends on the individual characteristics of the organism, which determine the degree of general and local reaction, as well as on the localization of the specific granuloma in the tissues of the maxillofacial area.

Actinomycosis most often occurs as an acute or chronic inflammatory process with exacerbations, characterized by a normergic reaction. When the disease lasts 2-3 months or more in persons burdened with concomitant pathologies (primary and secondary immunodeficiency diseases and conditions), actinomycosis becomes chronic and is characterized by a hypergic inflammatory reaction. Relatively rarely, actinomycosis occurs as an acute progressive and chronic hyperblastic process with a hyperergic inflammatory reaction.

Often the general hypergic chronic course is combined with local hyperblastic tissue changes, expressed in scar changes in the tissues adjacent to the lymph nodes, similar to muscle hypertrophy, hyperostotic thickening of the jaws.

Depending on the clinical manifestations of the disease and the characteristics of its course associated with the localization of a specific granuloma, it is necessary to distinguish the following clinical forms of actinomycosis of the face, neck, jaws and oral cavity: 1) cutaneous, 2) subcutaneous, 3) submucosal, 4) mucous, 5) odontogenic actinomycosis granuloma, 6) subcutaneous intermuscular (deep), 7) actinomycosis of the lymph nodes, 8) actinomycosis of the jaw periosteum, 9) actinomycosis of the jaws, 10) actinomycosis of the oral cavity - tongue, tonsils, salivary glands, maxillary sinus. (Classification by T. G. Robustova)

Skin form. Rarely seen. It occurs both odontogenically and as a result of damage to the skin. Patients complain of minor pain and thickening over a small area of ​​the skin; when questioned, they indicate a gradual enlargement and hardening of the lesion or lesions.

Actinomycosis of the skin occurs without an increase in body temperature. Upon examination, inflammatory infiltration of the skin is determined, one or more lesions growing outward are identified. This is accompanied by thinning of the skin, a change in its color from bright red to brown-blue. On the skin of the face and neck, pustules or tubercles may predominate, or a combination of both can occur.

The cutaneous form of actinomycosis spreads along the tissue.

Subcutaneous form characterized by the development of a pathological process in the subcutaneous tissue, usually near an odontogenic lesion. Patients complain of pain and swelling. From the anamnesis it can be found out that the subcutaneous form arose as a result of a previous purulent odontogenic disease. This form can also develop when the lymph nodes disintegrate and subcutaneous tissue is involved in the process.

The pathological process in this form of actinomycosis is characterized by a long but calm course. The period of decay of a specific granuloma may be accompanied by minor pain and low-grade fever.

Upon examination, a rounded infiltrate is detected in the subcutaneous tissue, initially dense and painless. During the period of granuloma disintegration, the skin adheres to the underlying tissues, becomes bright pink to red, and a softening area appears in the center of the lesion.

Submucosa form occurs relatively rarely, with damage to the oral mucosa - biting, foreign bodies, etc.

The form develops without a rise in body temperature. Pain in the affected area is moderate. Depending on the location, the pain may intensify when opening the mouth, talking, or swallowing. Then there is a feeling of a foreign body, awkwardness. On palpation, a dense infiltrate is determined to be round in shape, which is subsequently limited. The mucous membrane above it is soldered.

Actinomycosis of the mucous membrane mouth is rare. The radiant fungus penetrates through damaged mucous membranes; traumatic factors are most often foreign bodies, sometimes sharp edges of teeth.

Actinomycosis of the oral mucosa is characterized by a slow, calm course and is not accompanied by an increase in body temperature. The pain in the area is minor.

Upon examination, a superficially located inflammatory infiltrate with a bright red mucous membrane above it is determined. Often there is a spread of the lesion outward, its breakthrough and the formation of separate small fistulous tracts, from which granulations bulge.

Odontogenic actinomycosis granuloma It is rare in periodontal tissues, but is difficult to recognize. This lesion always tends to spread to other tissues. When the granuloma is localized in the skin and subcutaneous tissue, a cord is observed along the transitional fold, running from the tooth to the lesion in the soft tissues; with a submucosal lesion there is no cord. The process often spreads to the mucous membrane; with the next exacerbation, it becomes thinner, forming a fistulous tract.

Subcutaneous-intermuscular (deep) form actinomycosis is common. In this form, the process develops in the subcutaneous, intermuscular, interfascial tissue, spreading to the skin, muscles, jaw and other bones of the face. It is localized in the submandibular, buccal and parotid-masticatory areas, and also affects the tissues of the temporal, infraorbital, zygomatic areas, infratemporal and pterygopalatine fossae, pterygomaxillary and peripharyngeal spaces and other areas of the neck.

With a deep form of actinomycosis, patients indicate the appearance of swelling due to inflammatory edema and subsequent infiltration of soft tissues.

Often the first sign is a progressive limitation of mouth opening, since radiant fungi growing into the tissue affect the masticatory and internal pterygoid muscles, as a result of which a restriction in mouth opening that bothers the patient occurs.

On examination, the skin above the infiltrate appears bluish; foci of softening that arise in certain areas of the infiltrate resemble developing abscesses. A breakthrough in a thinned area of ​​skin leads to its perforation and the release of a viscous, purulent fluid, often containing small whitish grains - drusen of actinomycetes.

The acute onset or exacerbation of the disease is accompanied by an increase in body temperature to 38–39°C and pain. After opening the actinomycosis lesion, acute inflammatory phenomena subside. There is a board-like density of the peripheral parts of the infiltrate, areas of softening in the center with fistulous tracts. The skin over the affected area is welded together and cyanotic. Subsequently, the actinomycosis process develops in two directions: gradual resorption and softening of the infiltrate occurs or spread to neighboring tissues, which sometimes leads to secondary damage to the bones of the face or metastasis to other organs.

Actinomycosis lymph nodes occurs due to odontogenic, tonsillogenic, otogenic pathways of infection.

The process can manifest itself in the form of actinomycotic lymphangitis, abscessing lymphadenitis, adenophlegmon or chronic hyperplastic lymphadenitis.

The clinical picture of lymphangitis is characterized by a superficially located flat infiltrate, initially dense, and then softening and adhering to the skin. Sometimes the infiltrate occurs in the form of a dense cord running from the affected lymph node up or down the neck.

Abscessing actinomycotic lymphadenitis is characterized by complaints of a limited, slightly painful dense node. The disease develops sluggishly, without increasing body temperature. The lymph node is enlarged, gradually fuses with adjacent tissues, and tissue infiltration increases around it. When abscess formation occurs, the pain intensifies, the body temperature rises to low-grade fever, and malaise appears. After opening the abscess, the process undergoes reverse development, leaving a dense scar-altered conglomerate.

Adenophlegmon is characterized by complaints of sharp pain in the affected area; the clinic resembles the picture of phlegmon caused by a pyogenic infection.

With hyperplastic actinomycosis lymphadenitis, an enlarged, dense lymph node is observed, resembling a tumor or tumor-like disease. Characterized by a slow, asymptomatic course. The process may worsen and abscess.

Actinomycosis jaw periosteum is rare compared to other forms. It occurs in the form of exudative or productive inflammation.

With exudative periostitis of the jaw, inflammatory phenomena develop in the tooth area and spread to the vestibular surface of the alveolar process and the body of the jaw. Painful sensations are mild, well-being is not disturbed.

Clinically, a dense infiltrate develops in the vestibule of the oral cavity and smoothness of the lower fornix. The mucous membrane over it is red, sometimes with a bluish tint. Then the infiltrate slowly softens, is limited, and pain appears. Percussion of the tooth is painless, it seems to “spring”. When the lesion is opened, pus is not always released; granulations often grow.

With productive actinomycosis periostitis, thickening of the base of the lower jaw due to the periosteum is noted. The process from the periosteum of the alveolar part moves to the base of the jaw, deforming and thickening its edge.

X-ray examination reveals loose periosteal thickenings of a heterogeneous structure outside the alveolar part, the base of the jaw body, and especially along the lower edge.

Actinomycosis of the jaws. The pathological process with primary damage to the jaws is most often localized on the lower jaw and very rarely on the upper jaw. Primary actinomycosis of the jaw can be in the form of a destructive and productive-destructive process.

Primary destructive actinomycosis of the jaw can manifest itself as an intraosseous abscess or intraosseous gumma.

With an intraosseous abscess, patients complain of pain in the area of ​​the affected part of the bone. When the lesion is adjacent to the mandibular canal, sensitivity in the area of ​​the branching of the mental nerve is impaired. Subsequently, the pain becomes intense and acquires a neuralgic character. Swelling of the soft tissue adjacent to the bone appears.

The clinic of bone gumma is characterized by a slow, calm course with minor pain; accompanied by exacerbations in which inflammatory contracture of the masticatory muscles occurs.

Radiologically, primary destructive actinomycosis of the jaws is manifested by the presence in the bone of one or several fused cavities of a round shape, not always clearly contoured. With gumma, the lesion may be surrounded by a zone of sclerosis.

Primary productive-destructive damage to the jaws is observed mainly in children and adolescents, the cause is an odontogenic or tonsillogenic inflammatory process. There is thickening of the bone due to periosteal overlays, which progressively increases and thickens, simulating a neoplasm.

The course of the disease is long - from 1-3 years to several decades. Against the background of a chronic course, there are individual exacerbations, similar to those during a destructive process.

The x-ray shows new bone formation coming from the periosteum, compaction of the structure of the compact and spongy substance in the body area, and the branches of the lower jaw. Individual foci of resorption are detected; days of the cavity are small, almost punctate, others are large. Bone sclerosis is more or less pronounced around these lesions.

Actinomycosis of the oral cavity It is relatively rare and presents significant difficulties for diagnosis.

Clinic actinomycosis of tongue can occur in the form of a diffuse inflammatory process like phlegmon or abscess. A low-painful node appears on the back or tip of the tongue, which remains unchanged for a long time, and after 1-2 months. resolved by abscess formation and opening outward with the formation of fistulas and protrusion of abundant granulations.

Actinomycosis of the salivary glands can be primary and secondary. The clinical picture is varied; depending on the extent of the process in the gland and the nature of the inflammatory reaction, the following forms of actinomycosis of the salivary glands can be distinguished: 1) exudative limited and diffuse actinomycosis; 2) productive limited and diffuse actinomycosis; 3) actinomycosis of deep lymph nodes in the parotid salivary gland.

Diagnosis. Diagnosis of actinomycosis due to the significant diversity of the clinical picture of the disease presents some difficulties. The sluggish and prolonged course of odontogenic inflammatory processes and the failure of anti-inflammatory therapy are always alarming in relation to actinomycosis.

The clinical diagnosis of actinomycosis should be supported by a microbiological examination of the discharge, a skin allergy test with actinolysate and other immunodiagnostic methods, and a pathomorphological examination. In some cases, repeated, often multiple diagnostic studies are required.

Microbiological study of the discharge should consist of a study of the native preparation, a cytological study of stained smears and, in some cases, the isolation of a pathogenic culture by sowing.

The study of secretions in a native preparation is the simplest method for determining drusen and elements of radiant fungi. Cytological examination of stained smears makes it possible to establish the presence of actinomycete mycelium, secondary infection, and also to judge by the cellular composition the reactive abilities of the body (phagocytosis, etc.).

Differential diagnosis. Actinomycosis is differentiated from a number of inflammatory diseases: abscess, phlegmon, periostitis and osteomyelitis of the jaw, tuberculosis, syphilis, tumors and tumor-like processes. Clinical diagnosis is helped by microbiological studies, specific reactions, and serodiagnosis. Morphological data play an important role in the differential diagnosis of tumors.

Treatment. Therapy for actinomycosis of the maxillofacial area should be comprehensive and include: 1) surgical treatment methods with local effects on the wound process; 2) impact on specific immunity; 3) increasing the overall reactivity of the body; 4) impact on concomitant purulent infection; 5) anti-inflammatory, desensitizing, symptomatic therapy, treatment of concomitant diseases; 6) physical methods of treatment and exercise therapy.

Surgical treatment of actinomycosis consists of: 1) removal of teeth, which were the entry point for infection; 2) surgical treatment of actinomycosis foci in soft and bone tissues, removal of areas of excessively newly formed bone and, in some cases, lymph nodes affected by the actinomycosis process.

Wound care after opening an actinomycosis lesion is of great importance. Long-term drainage, subsequent scraping of granulations, treatment of affected tissues with 5% tincture of iodine, and administration of iodoform powder are indicated. When a secondary pyogenic infection occurs, deposited administration of antibiotics is indicated.

In case of normergic actinomycosis, actinolysate therapy is carried out or specially selected immunomodulators are prescribed, as well as restorative stimulants and, in some cases, biologically active drugs.

Therapy for actinomycosis with a hypergic inflammatory reaction begins with detoxification, restorative and stimulating treatment. Actinolysate and other immunomodulators are prescribed strictly individually. In order to relieve intoxication, a solution of hemodez, rheopolyglucin with the addition of vitamins, and cocarboxylase is injected intravenously. The complex for the treatment of chronic intoxication includes multivitamins with microelements, enterosorbents, and drinking plenty of fluids with infusions of medicinal herbs. This treatment is carried out for 7-10 days at intervals of 10 days in 2-3 courses. After 1-2 courses, immunomodulators are prescribed: T-activin, thymazine, actinolysate, staphylococcal toxoid, levamisole.

In case of a hyperergic type of process with pronounced sensitization to the radiant fungus, treatment begins with general antibacterial, enzymatic and complex infusion therapy aimed at correcting hemodynamics, eliminating metabolic disorders, and detoxification. Prescribed drugs that have desensitizing, restorative and tonic properties. Vitamins B and C, cocarboxylase, and ATP are used in the treatment complex. After a course of such treatment (from 2-3 weeks to 1-2 months), based on the data of an immunological study, a course of immunotherapy with actinolysate or levamisole is prescribed.

An important place in complex treatment is occupied by stimulating therapy: hemotherapy, the prescription of antigenic stimulants and restoratives - multivitamins, vitamins B1, B12, C, aloe extract, prodigiosan, pentoxyl, methyluracil, levamisole, T-activin, thymalin. Treatment should be combined with the prescription of antihistamines, pyrazolone derivatives, as well as symptomatic therapy.

Forecast for actinomycosis of the maxillofacial region, in most cases it is favorable.

Prevention. The oral cavity is sanitized and odontogenic and dental pathological lesions are removed. The main thing in the prevention of actinomycosis is to increase the general anti-infective defense of the body.

Tuberculosis is a chronic infectious disease caused by mycobacterium tuberculosis. Tuberculosis is a vector-borne disease. In recent years, the disease of the jaws, facial tissues and oral cavity has become rare.

Etiology. The causative agent of the disease is mycobacterium tuberculosis, thin, straight or curved rods, 1..10 microns long, 0.2..0.6 microns wide. There are three types of tuberculosis bacteria: human (causes 92% of cases of the disease), bovine (5% of cases) and an intermediate type (3%).

Pathogenesis. The source of the spread of infection is most often a person with tuberculosis, and the disease is transmitted through the nutritional route through the milk of sick cows. In the development of tuberculosis, a person’s immunity and resistance to this infection is of great importance.

It is customary to distinguish between primary and secondary tuberculosis lesions. Primary damage to the lymph nodes of the maxillofacial area occurs when mycobacteria enter through the teeth, tonsils, oral and nasal mucosa, and damaged skin. Secondary damage occurs when the primary affect is localized in other organs or systems.

Pathological anatomy. Tuberculosis can affect any organ or organ system, while remaining a general disease. At the site of entry of the pathogen, tuberculoma is formed - a banal inflammation develops, which in the proliferative phase acquires a specific character. A shaft of cellular elements is formed around the inflammatory focus, in which, in addition to cells characteristic of inflammation, there are epitheloid cells and giant Pirogov-Langhans cells. An area of ​​caseous necrosis forms in the center of the inflammatory focus. Another specific form of inflammation is a tubercle (tuberculous granuloma), morphologically similar to tuberculoma.

Clinical picture. In the maxillofacial area, lesions of the skin, mucous membranes, submucosa, subcutaneous tissue, salivary glands, and jaws are isolated.

Primary defeat lymphatic nodes characterized by their single appearance or in the form of soldered in a package. The lymph nodes are dense, and as the disease progresses they become even more dense, reaching a cartilaginous or bone consistency. In young patients, disintegration of the node is often observed with the release of a characteristic cheesy secretion. Primary tuberculosis of the lymph nodes is accompanied by general symptoms characteristic of the inflammatory process.

Secondary tuberculous lymphadenitis is one of the most common forms of this pathological process. It develops in the presence of a lesion in other organs. The disease often occurs chronically and is accompanied by low-grade fever, general weakness, and loss of appetite. In some patients, the process may have an acute onset, with a sharp increase in body temperature and symptoms of intoxication. There is an increase in lymph nodes; they have a dense elastic consistency, sometimes a bumpy surface, and are clearly contoured. Their palpation is slightly painful, sometimes painless. In some cases, rapid disintegration of the focus is observed, in others - slow suppuration with the formation of cheesy tissue disintegration. When the contents come out, a fistula or several fistulas remain. In recent years, the number of cases of slow-flowing lymphadenitis has increased.

Tuberculosis of the skin and subcutaneous tissue. There are several clinical forms:

Primary tuberculosis of the skin (tuberculous chancre) - erosions and ulcers with a compacted bottom form on the skin. Regional lymph nodes suppurate. After the ulcers heal, deforming scars remain.

Tuberculous lupus. The primary element is lupoma, which is characterized by the “apple jelly” symptom - when pressing on the lupoma with a glass slide, a yellow zone is formed in the center of the element. Lupomas have a soft consistency and tend to merge, forming an infiltrate, which, when resolved, forms deforming scars.

Scrofuloderma - most often forms in the immediate vicinity of a tuberculosis focus in the jaws or lymph nodes, less often - when the infection spreads from distant foci. Characteristic is the development of infiltrate in the subcutaneous tissue in the form of nodes or a chain of nodes, as well as fused gummous foci. The lesions are located superficially, covered with atrophic, thinned skin. The lesions open outward with the formation of single fistulas or ulcers, as well as their combinations. After autopsy, the affected tissues are characterized by a bright red or red-violet color. When the pus separates, a crust forms that covers the fistula or the surface of the ulcer. The process tends to spread to new tissue areas. After the lesions heal, characteristic atrophic star-shaped scars form on the skin.

Dissimilated miliary tuberculosis of the face is the appearance of small painless red or brown nodules on the skin of the face and neck, which can ulcerate and heal with the formation of a scar or without a trace.

Rosacea-like tuberculoid - against the background of rosacea-like redness and telangioectasias, pinkish-brown papules appear, rarely with pustules in the center. Opened pustules become crusty and heal with the formation of a scar.

Papulo-necrotic tuberculosis. Soft round papules with a diameter of 2-3 mm, non-peptic, cyanotic-brown in color, form on the skin. A pustule may form in the center of the papule, containing necrotic masses that dry out into a crust. Perifocal inflammation is observed around the papule.

Defeat by tuberculosis salivary glands is relatively rare. Tuberculosis bacteria spread into the gland hematogenously, lymphogenously, or, less commonly, by contact. The process is more often localized in the parotid gland, and there may be focal or diffuse damage; with tuberculosis of the submandibular gland - only diffuse. Clinically, the disease is characterized by the formation of dense, painless or slightly painful nodes in the gland. Over time, the skin over them becomes welded together. At the site of a break in a thinned area of ​​skin, fistulas or ulcerative surfaces form. The secretion of saliva from the gland duct is scanty or absent. When the lesion disintegrates and its contents empty into the duct, flocculent inclusions appear in the saliva. Sometimes paralysis of the facial muscles on the affected side may occur.

X-ray examination reveals foci of calcification in the projection of the salivary gland in the chain of lymph nodes. When sialography is observed, a blurred pattern of the gland ducts and individual stripes corresponding to the formed cavities are noted.

Tuberculosis of the jaws occurs secondarily, and also due to contact transition from the oral mucosa. Accordingly, they distinguish: a) bone damage in the primary tuberculosis complex; b) bone damage in active pulmonary tuberculosis.

Tuberculosis of the jaws is observed more often when the lungs are affected. It is characterized by the formation of a single focus of bone resorption, often with a pronounced periosteal reaction. On the upper jaw it is localized in the area of ​​the infraorbital margin or zygomatic process, on the lower jaw - in the area of ​​its body or branch.

At first, a tuberculosis lesion in the bone is not accompanied by pain, but as it spreads to other areas of the bone, periosteum, and soft tissue, pain and inflammatory contracture of the masticatory muscles appear. When the process moves from the depths of the bone to the adjacent tissues, infiltration, adhesion of the skin to the underlying tissues, and a change in its color from red to bluish are observed. One or more cold processes are formed, which are prone to spontaneous opening with the separation of watery exudate and lumps of cheesy decay, fused to the affected bone, leaving multiple fistulas with bulging granulations. Their probing makes it possible to detect a lesion in the bone filled with granulations, sometimes small dense sequesters. Slowly, such lesions completely or partially scar, leaving retracted, atrophic scars; tissue decreases, especially subcutaneous tissue. More often, fistulas persist for several years, with some fistulas scarring and new ones appearing nearby.

The radiograph reveals bone resorption and single intraosseous lesions. They have clear boundaries and sometimes contain small sequesters. When the disease is long-standing, the intraosseous lesion is separated by a zone of sclerosis from the healthy bone.

Diagnosis. Diagnosis of tuberculosis of the maxillofacial region consists of a number of methods and, first of all, tuberculin diagnostics, which makes it possible to establish the presence of tuberculosis infection in the body. Tuberculin solutions are used in various techniques (Mantoux, Pirquet, Koch tests). A general examination of patients is carried out using x-ray methods for examining the lungs. In addition, smears of pus from lesions, cell imprints from ulcers are examined, and cultures are isolated to detect tuberculosis bacteria.

Differential diagnosis. Primary and secondary damage to the lymph nodes must be differentiated from abscess, lymphadenitis, chronic osteomyelitis of the jaw, actinomycosis, syphilis, as well as from malignant neoplasms.

Scrofuloderma is differentiated from cutaneous and subcutaneous forms of actinomycosis, a cancerous tumor.

Tuberculosis damage to the jaw bones should be differentiated from the same processes caused by pyogenic microbes, as well as malignant neoplasms.

Treatment Patients with tuberculosis of the maxillofacial region are treated in a specialized hospital. General treatment should be supplemented by local: hygienic maintenance and sanitation of the oral cavity. Surgical interventions are carried out strictly according to indications: with the clinical effect of treatment and delimitation of the local process in the oral cavity, in bone tissue. Intraosseous lesions are opened, granulations are scraped out of them, sequesters are removed, fistulas are excised and ulcers are sutured or their edges are refreshed for tissue healing by secondary intention under a tampon of iodoform gauze. Teeth with periodontal disease affected by tuberculosis must be removed.

Forecast with timely general anti-tuberculosis treatment, favorable.

Prevention. The use of modern methods of treating tuberculosis is fundamental in the prevention of tuberculosis complications in the maxillofacial area. Treatment of caries and its complications, diseases of the mucous membrane and periodontium should be carried out.

SYPHILIS

Syphilis is a chronic infectious venereal disease that can affect all organs and tissues, including the maxillofacial area.

Etiology. The causative agent of syphilis is treponema pallidum (spirochete), a spiral-shaped microorganism, 4..14 µm long, 0.2..0.4 µm wide. In the human body it develops as a facultative anaerobe and is most often localized in the lymphatic system. The spirochete has little resistance to external factors.

There is no congenital or acquired immunity to syphilis.

Pathogenesis. Syphilis infection occurs through sexual contact. Treponema pallidum gets on the mucous membrane or skin, most often when their integrity is violated. Infection can also occur through non-sexual contact (domestic syphilis) or in utero from a sick mother.

Clinical picture. The disease has several periods: incubation, primary, secondary and tertiary. With congenital syphilis, specific changes are observed in the tissues of the maxillofacial area.

The primary period of syphilis is characterized by the appearance on the mucous membrane, including in the oral cavity, of primary syphiloma or chancre. In the secondary period of syphilis, the oral mucosa is most often affected, and pustular and roseolous elements are formed.

A rare manifestation of syphilis in the secondary period is damage to the periosteum. It is characterized by a slow and sluggish course. The thickened periosteum acquires a pasty consistency, but a periosteal abscess does not form. Gradually, areas of the periosteum become denser, and flat elevations appear.

The tertiary period of syphilis develops 3-6 years or more after the onset of the disease and is characterized by the formation of so-called gummas. Gummas can be localized in the mucous membrane, periosteum and bone tissue of the jaws. Manifestations of syphilis in the tertiary period do not always occur; therefore, manifest or latent tertiary syphilis is distinguished.

When syphilitic gummas form, a dense, painless nodule first appears, which eventually opens with rejection of the gumma core. The resulting ulcer has a crater-shaped shape and is painless on palpation. Its edges are smooth, dense, the bottom is covered with granulations.

Syphilitic lesion of the tongue manifests itself in the form of gummous glossitis, diffuse interstitial glossitis.

Damage to the periosteum in the tertiary period of syphilis is characterized by diffuse, dense infiltration of the periosteum. Next, the thickened periosteum is fused with the mucous membrane, and in the area of ​​the body of the jaw - with the skin; The gumma softens and opens outward, forming a fistula or ulcer in the center. The ulcer on the periosteum of the jaw gradually scars, leaving thickenings on the surface, often ridge-shaped. The teeth may be involved in the process, they become painful and mobile. The process of periosteum can transfer to the bone.

Changes in bone tissue during the tertiary period of syphilis are localized in the area of ​​the jaws, nasal bones, and nasal septum. The process begins with thickening of the bone, increasing as the gumma grows. The patient experiences severe pain and sometimes sensory disturbances in the area of ​​the branching of the mental, sub- and supraorbital nasopalatine nerves. Subsequently, the gumma grows in one or several places to the periosteum, mucous membrane or skin, opens outward, forming fistula tracts. Sequesters are not always formed; they are small. Only the addition of a secondary pyogenic infection leads to necrosis of larger areas of the bone. In this case, communications with the nasal cavity and maxillary sinus may form on the upper jaw.

After the gumma disintegrates in the bone, gradual tissue healing occurs with the formation of rough, dense, often constricting scars. Exostoses and hyperostoses develop in the bone.

The X-ray picture of gummous bone lesions is characterized by foci of destruction of various sizes with clear, smooth edges, surrounded by sclerotic bone tissue.

Diagnosis. The clinical diagnosis of syphilis is confirmed by the Wasserman reaction and other serological reactions. Microbiological examination, as well as morphological examination of the affected tissues, is important.

Differential diagnosis Syphilitic lesions of the oral cavity, teeth and jaws pose certain difficulties. The ulcerative form of primary syphiloma on the lip may resemble a disintegrating cancerous tumor. Gummas of the oral mucosa have common symptoms with traumatic ulcers. Gummy glossitis should be differentiated from a tuberculous ulcer or cancerous lesion.

Syphilitic lesions of the periosteum and bone tissue should be distinguished from nonspecific and specific lesions of these tissues. The gummous process in the bone can simulate cancer or sarcomatous diseases.

Treatment syphilis is carried out in a specialized venereology hospital.

If syphilis affects the bone tissue of the jaws, periodic studies of the electrical excitability of the dental pulp are advisable; according to indications, trepanation of teeth with dead pulp and treatment according to the principle of therapy for chronic periodontitis. Movable teeth should not be removed; after treatment, they are quite well strengthened.

Active surgical treatment for damage to the periosteum of the jaws due to syphilis is not indicated even in the case of sequestration formation. They are removed after specific treatment as the process subsides.

Hygienic maintenance of the oral cavity is important. Tartar is removed, sharp edges of teeth are polished, and the oral cavity is sanitized.

Forecast with timely diagnosis, proper treatment and further clinical observation, it is generally favorable.

Prevention. In the prevention of syphilis, in addition to its social aspect, hygienic maintenance of the oral cavity, prevention of cracks and erosions in it are important.

USED ​​BOOKS:

1) “Surgical dentistry” - ed. Robustova. M. Medicine, 1996 With. 295-308.

2) “Surgical dentistry” edited by V. A. Dunaevsky - M. Medicine, 1979. With. 221-224

3) “Guide to maxillofacial surgery and surgical dentistry” - A.A. Timofeev. Kyiv, “Chervona Ruta Tours”, 1997. With. 345-350.